【Animal Modeling】-Lung injury rat model

  Objective: How to use a variety of combustible and temperature-controlled composite materials to establish a rat model of smoke inhalation acute lung injury?

  Method: Design a separate smoke box and engine room simulation box. Is the rat trapped in a dangerous cage in a designated area of the cabin simulation box? During the experiment, has the amount of smoke in the test box been detected and controlled to achieve the goal of stabilizing the damage coefficient? The experiment was carried out in two parts. The first part was the different smoking time groups, and the 48-hour survival rate of each group was observed. The second part is to choose 30 minutes of smoke inhalation as the cause of the injury, and analyze the blood gas, lung injury pathology score, alveolar lavage fluid and peripheral blood white blood cells 6 to 24 hours after inhaling the smoke. Inflammatory factors? The main signal transduction factor in the signal transduction pathway? Can changes in liver and kidney function be detected?

  Results: 1) The survival rates of various smoke inhalation time groups were 84.21% (15 minutes group); 25% (30 minutes group), 0 ((50 minutes group)); (2) Carboxyhemoglobin, carbon dioxide partial pressure , The lactic acid level increased significantly within 1 hour after inhaling smoke 30 minutes (P\u003c0.05), and then gradually returned to normal levels; compared with the control group, lung injury scores were scored at 6 hours and 24 hours after smoke inhalation (LIS)? The protein content of alveolar lavage fluid (BALF) increased significantly, and the total number of white blood cells in BALF increased significantly after inhaling smoke. The proportion of alveolar macrophages first decreased and then increased, and high neutrophils and neutrophils first increased and then decreased; different studies of different inflammatory factors and signal pathways have found that the activation of various signal transduction factors can be inhaled It occurs within 1 hour of qi, and WB and immunofluorescence indicate that activation is most important at 6 hours and 24 hours. Will it gradually decrease in the future? Are there any specific changes in liver and kidney function after inhaling smoke?

  Conclusion: A stable, reliable and deadly simulated ship fire smoke inhalation lung injury model has been established. There are multiple inflammatory pathways in the acute phase of smoke inhalation. The extensive activation and typical inflammatory cell changes and lung injury characteristics have laid a foundation for further research basis.